Signs and symptoms of dehydration usually warrant going to a hospital's emergency department. Infants, especially under 6 weeks of age or if the infant appears to slow urine output or decrease fluid intake, should be evaluated by their pediatrician or in an emergency center if oral sores appear. Individuals with immune suppression (for example, patients undergoing chemotherapy, HIV patients, or cancer patients) should contact their doctors if they suspect a HSV-1 infection.
Until the 1980s serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice.[39] The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, a glycoprotein G-specific (IgG) HSV test introduced in the 1980s is more than 98% specific at discriminating HSV-1 from HSV-2.[40]
HSV-2 is commonly referred to as genital herpes because it usually causes cold sores to erupt around the genitalia. In fact, genital herpes is the No. 1 cause of genital ulcers worldwide, according to the Centers for Disease Control and Prevention (CDC), and affects up to 1 in 3 adults (although most who are infected don’t even know it). (5) Both types of herpes viruses are highly contagious, and both can cause cold sores in either area of the body (or sometimes both). 
These herpes viruses enter the body through small cuts, abrasions, or breaks in the skin or mucous membranes. The incubation period for herpes simplex infections is about three to six days. Transmission (spread) of the virus is person to person and more likely to occur if blisters or lesions are present. The majority enter after an uninfected person has direct contact with someone carrying the virus (either with or without noticeable lesions). Simply touching an infected person is often the way children get exposed. Adolescents and adults frequently get exposed by skin contact but may get their first exposure by kissing or sexual contact (oral and/or genital contact), especially for HSV-2. Statistical studies suggest that about 80%-90% of people in the U.S. have been exposed to HSV-1 and about 30% have been exposed to HSV-2. Usually, the contagious period continues until lesions heal. Some people (estimated from 30%-50%) occasionally shed herpes virus while having few or no associated symptoms or signs.
The most common reason that people develop cold sores on their mouths is due to becoming infected with HSV-1. (4) HSV-1 usually causes cold sore breakouts around the lips or mouth, or what some people describe as “fever blisters.” Someone can become infected with HSV-1 starting as a child, and then the virus can lay dormant in the body until the immune system is weakened, at which point symptoms can surface.
While some people realize that they have genital herpes, many do not. It is estimated that one in five persons in the United States has genital herpes; however, as many as 90 percent are unaware that they have the virus. This is because many people have very mild symptoms that go unrecognized or are mistaken for another condition or no symptoms at all.
Herpes antiviral therapy began in the early 1960s with the experimental use of medications that interfered with viral replication called deoxyribonucleic acid (DNA) inhibitors. The original use was against normally fatal or debilitating illnesses such as adult encephalitis,[92] keratitis,[93] in immunocompromised (transplant) patients,[94] or disseminated herpes zoster.[95] The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C,[96] later marketed under the name cytosar or cytarabine. The usage expanded to include topical treatment of herpes simplex,[97] zoster, and varicella.[98] Some trials combined different antivirals with differing results.[92] The introduction of 9-β-D-arabinofuranosyladenine, (ara-A or vidarabine), considerably less toxic than ara-C, in the mid-1970s, heralded the way for the beginning of regular neonatal antiviral treatment. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the U.S. Food and Drug Administration in 1977. Other experimental antivirals of that period included: heparin,[99] trifluorothymidine (TFT),[100] Ribivarin,[101] interferon,[102] Virazole,[103] and 5-methoxymethyl-2'-deoxyuridine (MMUdR).[104] The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA aciclovir, in the late 1970s[105] raised antiviral treatment another notch and led to vidarabine vs. aciclovir trials in the late 1980s.[106] The lower toxicity and ease of administration over vidarabine has led to aciclovir becoming the drug of choice for herpes treatment after it was licensed by the FDA in 1998.[107] Another advantage in the treatment of neonatal herpes included greater reductions in mortality and morbidity with increased dosages, which did not occur when compared with increased dosages of vidarabine.[107] However, aciclovir seems to inhibit antibody response, and newborns on aciclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.[107]
At least 80 to 90 percent of people in the U.S. have already been exposed to the HSV-1 virus.sup style="font-size: 10px;">21 Meanwhile, around 3.7 billion HSV-1 infections were recorded in 2012 all over the world, according to the World Health Organization. Africa was home to the highest number of cases, with 87 percent of occurrences coming from this continent.22
The most effective method of avoiding genital infections is by avoiding vaginal, oral, and anal sex.[1] Condom use decreases the risk.[1] Daily antiviral medication taken by someone who has the infection can also reduce spread.[1] There is no available vaccine[1] and once infected, there is no cure.[1] Paracetamol (acetaminophen) and topical lidocaine may be used to help with the symptoms.[2] Treatments with antiviral medication such as aciclovir or valaciclovir can lessen the severity of symptomatic episodes.[1][2]
Herpes virus type 4 is also called Epstein-Barr virus. It typically causes infectious mononucleosis, a “kissing” disease. Symptoms include skin rash, fever, sore throat and swollen lymph glands. The virus can be involved in cancers like nasopharyngeal cancer. Herpes virus type 4 is contagious through bodily fluids, including saliva. Kissing, coughing, sneezing, or sharing utensils can make the infection spread.

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The flares are caused when your immune system falters. This can be due to a number of reasons. Anything from daily stressors, lack of sleep, poor nutrition, weight gain, concurrent illnesses etc may cause your immune system to be distracted from the Herpes Simplex Virus (HSV) infection. The moment that happens, the virus will flare resulting in rashes, cold sores, ulcers or blisters on your body.
Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.[70]
According to Melissa King, a psychotherapist who runs a support group for women with herpes in New York City, when someone finds out they’ve gotten herpes from a partner, there’s often immediately an assumption that the partner knew that they had it and lied, or that they were cheating. “But the reality is that in a lot of cases, people don’t know that they have it,” King tells BuzzFeed.
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